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Lookup NU author(s): Dr Hayden Homer, Aaron McDougall, Dr Mark Levasseur, Professor Mary Herbert
In mammalian somatic cells, the spindle assembly checkpoint (SAC) is indispensable for ensuring the fidelity of chromosome segregation by delaying cell-cycle progression in the face of even a single misaligned chromosome. In contrast, the role of the SAC in unperturbed mammalian oocytes is less well defined as progression through meiosis I is unaltered in mouse oocytes in the presence of one or a few misaligned chromosomes. Furthermore, attempts to disable the function of the SAC protein, Mad2, in mouse oocytes have produced conflicting results. To gain further insight into SAC function during female mammalian meiosis I, we recently utilised a morpholino-based antisense approach to deplete the majority of Mad2 in mouse oocytes. Our results define a clear role for Mad2 in ensuring the proper timing of meiosis I events and ultimately, in ensuring the fidelity of homologue disjunction. We discuss the implications of these results for the regulation of meiosis I in mammalian oocytes and for the genesis of human aneuploidy. ©2005 Landes Bioscience.
Author(s): Homer HA, McDougall A, Levasseur M, Herbert M
Publication type: Note
Publication status: Published
Journal: Cell Cycle
Year: 2005
Volume: 4
Issue: 5
Pages: 650-653
Print publication date: 01/05/2005
ISSN (print): 1538-4101
ISSN (electronic): 1551-4005
URL: http://www.landesbioscience.com/journals/6/article/1677/
PubMed id: 15846076
